Effect of chronic sustained hypoxia on NPR-A, NPR-B, MAP-2 and GFAP expressions in cerebral cortex and hippocampus.

Chronic sustained hypoxia affects various mechanisms depending on changes in blood flow in the brain. The natriuretic peptide system acts as a modulatory regulator of blood pressure and body fluid homeostasis. This study aimed to evaluate the expressions of natriuretic peptide receptor (NPR) and monoamine oxidase levels in rats' cerebral cortex and hippocampus under chronic sustained hypoxia. Groups; Sham: Rats exposed to 21 % O2 in a normobaric chamber for 1 week. Moderate-chronic sustained hypoxia (mCSH): Rats exposed to 13 % O2 ​​in a normobaric chamber for 1 week. Severe-chronic sustained hypoxia (sCSH): Rats exposed to 10 % O2 in a normobaric chamber for 1 week. Significant histopathological changes occurred in the cerebral cortex and hippocampus. NPR-A and NPR-B immunoreactivities increased in the hypoxia groups. Hypoxia decreased microtubule-associated protein-2 (MAP-2) immunoreactivity while increasing glial fibrillary acidic protein (GFAP) immunoreactivity. Monoamine oxidase was upregulated in sCSH. The NPR system is one of the mechanisms affected by hypoxia-induced damage in parallel with the degree of hypoxia. The use of natriuretic peptides or monoamine oxidase inhibitors against hypoxia exposure will serve to increase the potential efficacy of therapeutic interventions.